The Protective Effects of Trehalose on Gene Expression Linked to Oxidative Stress and Inflammation in Liver Tissue of Adult and Aged Wistar Rats
Background: Aging is associated with chronic diseases and increased oxidative stress, particularly affecting liver function. Aging is linked to chronic diseases and heightened oxidative stress, particularly impacting liver function. Recent research has demonstrated that oral administration of trehalose offers multiple benefits for various tissues and organs.Methods: This study investigated the effects of oral trehalose (2% in water) on the gene expression of key markers linked to liver oxidative stress and inflammation in 4-month-old adult and 24-month-old Wistar rats. Thirty-two male Wistar rats (n = 8) were randomly assigned into four groups: adult control, aged control, adult trehalose (2% in water), and aged trehalose, over a treatment period of one month. Following treatment, liver tissues were analyzed using real-time PCR for genes related to oxidative stress (PGC-1α, NRF2, and SOD) and inflammation (NF-κB, IL-1β, TNF-α, and TGF-β).Results: Our findings revealed a significant up-regulation of PGC-1α, NRF2, and SOD in aged trehalose group compared to the aged control (P < 0.001); however, SOD expression increased by trehalose administration in aged rats compared to other 3 groups. Inflammatory markers (NF-κB, IL-1β, TNF-α) were significantly reduced by trehalose, and TGF-β expression, involved in fibrosis, was attenuated exclusively in aged rats compared with controls (P < 0.05).Conclusion: These results suggest that trehalose has a protective effect on hepatic function, particularly in the aging population, and highlight its potential therapeutic role in age-associated liver dysfunction.
Normalization of Immune Response via Chondroitin Sulfate and Fucoidan Targeting N-Acetylgalactosaminidase
This review explores the pharmacological potential of chondroitin sulfate and fucoidan as immunomodulatory agents targeting N-acetylgalactosaminidase (nagalase) to normalize immune responses. Nagalase, an enzyme produced by tumor and virus-infected cells, contributes to immune suppression by deactivating macrophage-activating factor. Both chondroitin sulfate and fucoidan, as representatives of glycosaminoglycans and heteropolysaccharides, exhibit significant potential in inhibiting nagalase activity, thereby restoring immune functionality. Chondroitin sulfate, a key component of the extracellular matrix, demonstrates anti-inflammatory and tissue-regenerative properties by modulating nuclear factor (NF)-κB pathways and cytokine expression. Fucoidan, a sulfated polysaccharide derived from brown seaweed, enhances immune responses through macrophage and natural killer cell activation, while also exhibiting antiviral and anticancer activities. This dual action positions these compounds as promising agents for therapeutic interventions in chronic inflammatory conditions, cancer, and infectious diseases. The synergistic effects of chondroitin sulfate and fucoidan highlight their potential to address the root causes of immune dysregulation. This review aims to elucidate the underlying mechanisms of action and explore the clinical applications of these compounds within the framework of innovative immunotherapeutic strategies. However, current evidence is limited by the predominance of preclinical studies and variability in experimental models. Well-designed clinical trials are needed to validate their efficacy for therapeutic use.
Normalization of Immune Response via Chondroitin Sulfate and Fucoidan Targeting N-Acetylgalactosaminidase
This review explores the pharmacological potential of chondroitin sulfate and fucoidan as immunomodulatory agents targeting N-acetylgalactosaminidase (nagalase) to normalize immune responses. Nagalase, an enzyme produced by tumor and virus-infected cells, contributes to immune suppression by deactivating macrophage-activating factor. Both chondroitin sulfate and fucoidan, as representatives of glycosaminoglycans and heteropolysaccharides, exhibit significant potential in inhibiting nagalase activity, thereby restoring immune functionality. Chondroitin sulfate, a key component of the extracellular matrix, demonstrates anti-inflammatory and tissue-regenerative properties by modulating nuclear factor (NF)-κB pathways and cytokine expression. Fucoidan, a sulfated polysaccharide derived from brown seaweed, enhances immune responses through macrophage and natural killer cell activation, while also exhibiting antiviral and anticancer activities. This dual action positions these compounds as promising agents for therapeutic interventions in chronic inflammatory conditions, cancer, and infectious diseases. The synergistic effects of chondroitin sulfate and fucoidan highlight their potential to address the root causes of immune dysregulation. This review aims to elucidate the underlying mechanisms of action and explore the clinical applications of these compounds within the framework of innovative immunotherapeutic strategies. However, current evidence is limited by the predominance of preclinical studies and variability in experimental models. Well-designed clinical trials are needed to validate their efficacy for therapeutic use.
D-Allulose Improves Mitochondrial Respiratory Function and Alleviates Obesity-Induced Liver Dysfunction: A Comparative Study with Erythritol in HFD-Fed Mice - ScienceDirect
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New video: Hebrew Bible vs. Greek Bible - Numbers (Amounts) in the Greek Septuagint
Shalom ${contact.name.first}, Over the years many people have contacted us with questions regarding the Greek Septuagint (LXX) versus the Hebrew Masoretic Text (MT). There is a heated debate about the reliability and accuracy of the Hebrew Masoretic Text, and a growing number of Bible believers are now relying on the second-hand Greek LXX translation rather than on the original Hebrew text. In this video, we investigate the claims of Dr. Henry B. Smith, who maintains that the Greek LXX has preserved the correct and original chronology, while the chronology of the Hebrew MT has allegedly been corrupted by over 1,000 years! Thankfully, this debate can be settled with clear evidence from the Biblical narrative itself! By calculating Methuselah's age with regards to the flood, we can show very clearly which version is correct and which version is corrupt. We also respond to a well-known counter argument on this topic. Watch this video if you would like to know which version of the Tanach (Old Testament) has been corrupted and which version can be trusted: Hebrew Bible vs. Greek Bible - Numbers (Amounts) in the Greek Septuagint
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The Charlie Kirk Redemption: The Meaning, The Future, & The Answer | Jonathan Cahn Prophetic - YouTube
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3430 Year Clock INSTANTLY Proves Year & Day Jesus Returns (You'll See It!) - YouTube
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NEW STUDY: Cell Phone Radiation at 20× Below Legal Limit Induced Brain Damage in Rats
Infant rats exposed to “safe” cell phone radiation levels suffered impaired neuronal development and disrupted brain chemistry, while parallel in-vitro tests showed DNA damage in neural stem cells.
ELECTRICAL POISONING: THE HIDDEN EMF THREAT - The HighWire
With cell phones in our pockets, Wi-Fi routers in nearly every home, and smart devices all around us, concern over electromagnetic fields (EMFs) is growing. Dr. Carlos Ritter joins Del to break down what the science really shows about EMF exposure and its potential impact on human health. Ritter doesn’t stop at raising an alarm; […]
BREAKING STUDY: First Direct Evidence of mRNA "Vaccine" Genomic Integration Identified in Stage IV Cancer Patient
Vaccine DNA plasmid-derived Spike gene sequence integrated into chromosome 19 with perfect 20/20 bp identity — accompanied by widespread genomic dysfunction.
mRNA "Vaccine" Genomic Integration: Visualized in Hyper-Realistic Detail
Sentinel case of a young stage IV bladder cancer patient reveals a vaccine-derived Spike gene sequence embedded in chromosome 19 with a perfect 20/20 bp match.
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Unlock the truth about mRNA vaccines with Christie Grace MSc, and discover what’s really inside — information that could take down the entire platform. This ...